血脂異常誘發心臟電氣生理及機械功能失全之病生理機轉
Date Issued
2000
Date
2000
Author(s)
吳造中
DOI
892314B002118
Abstract
In this study project, single ventricular myocytes isolated from hyper- & normocholesterolemic
rabbits were used to define the amplitude and duration of action potential in hypercholesterolemic
status and to study the hyperlipidemic effect on the magnitude of calcium inward and potassium
outward currents, which are two major currents responsible for the duration of action potential.
The cell capacitance was 108+8.2 pF in normolipidemic myocytes (n=125) and 162+8.2 pF
(n=118) in hypercholesterolemic cells (p<0.05). There were no significant difference of the resting
membrane potential (-70.4+9.4 vs. –73.4+12.3 mV, p=NS) and the amplitude of action potential
(115.2+24.1 vs. 13.2+16.7 mV, p=NS) between the hypercholesterolemic myocytes (n=18) and normal
controls (n=11). However, the phase 0 depolarization of action potential was slower (54.8+32.1 vs.
80.7+16.2 V/s, p<0.02) and the action potential duration was longer (APD: 206.2+77.7 vs. 137.6+74.7
ms, APD90: 196.9+79.0 vs. 135.0+70.5 ms, and APD50: 173.2+82.2 vs. 112.5+68.9 ms, respectively,
p<0.05). While the peak I Ca was larger in the hypercholesterolemic myocytes, capacitative surface
area was also larger; thus there were no differences in the peak current densities between these two
groups. While there was no difference in the peak currents, Ito density was significantly smaller in the
hypercholesterolemic myocytes.
In conclusion, the findings of the present experiments suggested that hypercholesterolemia
associated changes in action potential resulted from the decrease in I Na and Ito density.
rabbits were used to define the amplitude and duration of action potential in hypercholesterolemic
status and to study the hyperlipidemic effect on the magnitude of calcium inward and potassium
outward currents, which are two major currents responsible for the duration of action potential.
The cell capacitance was 108+8.2 pF in normolipidemic myocytes (n=125) and 162+8.2 pF
(n=118) in hypercholesterolemic cells (p<0.05). There were no significant difference of the resting
membrane potential (-70.4+9.4 vs. –73.4+12.3 mV, p=NS) and the amplitude of action potential
(115.2+24.1 vs. 13.2+16.7 mV, p=NS) between the hypercholesterolemic myocytes (n=18) and normal
controls (n=11). However, the phase 0 depolarization of action potential was slower (54.8+32.1 vs.
80.7+16.2 V/s, p<0.02) and the action potential duration was longer (APD: 206.2+77.7 vs. 137.6+74.7
ms, APD90: 196.9+79.0 vs. 135.0+70.5 ms, and APD50: 173.2+82.2 vs. 112.5+68.9 ms, respectively,
p<0.05). While the peak I Ca was larger in the hypercholesterolemic myocytes, capacitative surface
area was also larger; thus there were no differences in the peak current densities between these two
groups. While there was no difference in the peak currents, Ito density was significantly smaller in the
hypercholesterolemic myocytes.
In conclusion, the findings of the present experiments suggested that hypercholesterolemia
associated changes in action potential resulted from the decrease in I Na and Ito density.
Subjects
血脂異常
電氣-機械功能
動作電位
鈣離子孔道
鉀離子孔道
Dyslipidemia
Electromechanical function
Action potential
Calcium channel
Potassium
channel
channel
Intracellular calcium
Publisher
臺北市:國立臺灣大學醫學院內科
Type
report
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